The perirhinal cortex (PRh) is important because (i) it is the gateway to the hippocampus and amygdala; (ii) it has been shown to have an extremely low seizure threshold, a fact than could afford important insights into the causes and treatment of epilepsy, (iii) it is among the first cortical regions to exhibit anatomical signs associated with Alzheimer's disease, so that knowing more about its cellular and molecular neurobiology could point tot he causes and treatment of age-related cognitive disorders; and (iv) recent evidence suggests a key role for the PRh in certain mnemonic functions previously associated with the amygdala and/or hippocampus. Essentially nothing is known about the cellular neurophysiology of PRh neurons and their functional relationship to and interactions with cells of the lateral amygdala (LA), an adjacent brain region that has reciprocal connections to PRh and has been implicated in emotional learning. The present research uses new technology that I helped to develop and apply to rat brain slices that will test interesting hypotheses and afford key insights into the cellular neurobiology of PRh and LA during development and aging. The first goal is to use this new technology to create a library of cell types that includes both physiology and morphology. These quantitative data will test the hypothesis that LA can be regarded as "cortex-like" in the sense of resembling the adjacent PRh. The second goal is to use this background information to explore the kinds of use-dependent synaptic plasticity exhibited between these two brain regions. The results could furnish the cellular mechanisms for hypotheses derived from behavioral studies regarding the mnemonic functions of LA and PRh and their relationships. The third goal is to examine changes in the cellular neurobiology and synaptic plasticity as a function of normal development and aging. The initial aging studies will focus on further advances in the methodology that will allow us to examine more conveniently tissue obtained from older animals, which is notoriously more difficult. The working hypothesis is that certain of the age-related neuronal changes -- including those pertinent both to cognitive dementias and to the search for cognitive enhancers -- involve changes in calcium homeostasis. In addition to testing interesting hypothesis is that certain of the age- related neuronal changes -- including those pertinent both to cognitive dementias and to the search for cognitive enhancers --involve changes in calcium homeostasis. In addition to testing interesting hypotheses about this largely uncharted area, the data and technology will be vital for further understanding at a cellular and molecular level age-related dementias and the actions of cognitive enhancers in these brain regions. In the next stage of my career, as a postdoctoral fellow and then as an independent researcher, I plan to build on this foundation to explore further the cellular and molecular mechanisms and possible treatments for age-related cognitive dysfunction, particularly memory. This is not a field that will suffer fleeting interest.